Apoptosis of leukocytes triggered by acute DNA damage promotes lymphoma formation

被引：92
|
作者：
Labi, Verena [1 ]
Erlacher, Miriam [1 ,2 ]
Krumschnabel, Gerhard [1 ]
Manzl, Claudia [1 ]
Tzankov, Alexandar [3 ]
Pinon, Josephina [4 ]
Egle, Alexander [4 ]
Villunger, Andreas [1 ]
机构：
[1] Innsbruck Med Univ, Div Dev Immunol, Bioctr, A-6020 Innsbruck, Austria
[2] Univ Hosp Freiburg, Dept Pediat & Adolescent Med, Div Pediat Hematol & Oncol, D-79106 Freiburg, Germany
[3] Univ Basel, Inst Pathol, CH-4031 Basel, Switzerland
[4] Paracelsus Med Univ, Lab Immunol & Mol Canc Res, Dept Med 3, A-5020 Salzburg, Austria
来源：
GENES & DEVELOPMENT | 2010年 / 24卷 / 15期
基金：
奥地利科学基金会;
关键词：
Apoptosis; p53; BH3-only proteins; stem cells; gamma-irradiation; cancer; PROTECTS HEMATOPOIETIC STEM; SELF-RENEWAL; PUMA; CELLS; P53; SUPPRESSOR; PATHWAY; BIM; EXPRESSION; DELETION;
D O I：
10.1101/gad.1940210
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Apoptosis triggered by p53 upon DNA damage secures removal of cells with compromised genomes, and is thought to prevent tumorigenesis. In contrast, we provide evidence that p53-induced apoptosis can actively drive tumor formation. Mice defective in p53-induced apoptosis due to loss of its proapoptotic target gene, puma, resist gamma-irradiation (IR)-induced lymphomagenesis. In wildtype animals, repeated irradiation injury-induced expansion of hematopoietic stem/progenitor cells (HSCs) leads to lymphoma formation. Puma(-/-) HSCs, protected from IR-induced cell death, show reduced compensatory proliferation and replication stress-associated DNA damage, and fail to form thymic lymphomas, demonstrating that the maintenance of stem/progenitor cell homeostasis is critical to prevent IR-induced tumorigenesis.
引用
收藏
页码：1602 / 1607
页数：6
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